Management of Cardiac Arrest

Dr. Michael J. Baffsky

Intensive Care Registrar

Concord ICU

Concord Hospital

23rd February 2004

Definition of Cardiac Arrest

• Abrupt cessation of cardiac pump function which may be reversible by a prompt intervention but will lead to death in its absence

• Sudden Cardiac Death is the most common cause of sudden natural death

Definition of Cardiac Arrest

• Out Of Hospital

• In Hospital

Incidence

• 1 in 100,000 per year in young adults

• 1 in 1000 per year in aged 45-75

Causes Of Cardiac Arrest

Coronary heart disease (most common)

Myocardial hypertrophy

Cardiac inflammatory diseases

Cardiac valvular disease

Electrophysiologic Abnormalities (e.g. WPW)

Electrolyte disturbances

Abnormal metabolic states

Sympathetic nervous system disorders

Proarrhythmic toxic exposures

Electrocution

Tension pneumothorax

Trauma

Drowning

Pulmonary embolism

Causes Of Cardiac Arrest

Coronary heart disease (most common)

Myocardial hypertrophy

Cardiac inflammatory diseases

Cardiac valvular disease

Electrophysiologic Abnormalities (e.g. WPW)

Electrolyte disturbances

Abnormal metabolic states

Sympathetic nervous system disorders

Proarrhythmic toxic exposures

Electrocution

Tension pneumothorax

Trauma

Drowning

Pulmonary embolism

Causes Of Cardiac Arrest

Coronary heart disease (most common)

Myocardial hypertrophy

Cardiac inflammatory diseases

Cardiac valvular disease

Electrophysiologic Abnormalities (e.g. WPW)

Electrolyte disturbances

Abnormal metabolic states

Sympathetic nervous system disorders

Proarrhythmic toxic exposures

Electrocution

Tension pneumothorax

Trauma

Drowning

Pulmonary embolism

Are Arrests Predictable?

• Genetic– general– specific

• Congenital long QT interval syndromes

• Right ventricular dysplasia

• Brugada Syndrome (RBBB with non-ischemic ST-segment elevations

Survival Of A Cardiac Arrest

• <5% of people survive an “out of hospital” arrest

• Statistics vary on “in hospital” arrests

The 'chain of survival' concept

• To improve survival in an arrest:- Recognition of the cardiac arrest Early activation of emergency services Early basic life support Early defibrillation Early advanced life support

How Does An Arrest Present?

• Patient found, usually unconscious– most often by a nurse

• An arrest is called– (Do YOU know the emergency number?)

• BLS should commence immediately

• The nature of the arrest identified quickly

• Appropriate action should be taken

How Does An Arrest Present?

• Ventricular Fibrillation/Flutter (60%-80%)

• Ventricular Tachycardia– Conscious and Unconscious (Pulseless)

• Supraventricular Tachycardia

• Pulseless Electrical Activity (EMD) (~10%)

• Cardiac Standstill (Asystole) (20%-40%)– More difficult to treat with worse prognosis

Ventricular Fibrillation (VF)

• Survivability decreases by 10% per minute until normal rhythm restored

• Coarse or fine

• Fine may looks like asystole– Could be equipment gain– If any doubt, shock

Ventricular Fibrillation

Ventricular Tachycardia (VT)

• Conscious– Treat pharmacologically

• Unconscious– Treat as for VF

AF with WPW

Causes of Pulseless Activity

• PE• Hypovolaemia• Acidosis

• Tension PTx• Cardiac Tamponade• Hypoxaemia

Treat the cause

Asystole

• Impaired automaticity of SA node

• Problems with conduction pathways– usually due to ischaemia/hypoxea

• Sympathetic reflex failure

• Acidotic and Ischaemic Environment– may affect the efficacy of adrenalin

Will My Efforts Be Successful?

• The probability of achieving successful resuscitation from cardiac arrest is related to the interval from onset to institution of resuscitative efforts, the setting in which the event occurs, the mechanism (VF, VT, PEA, asystole) and the clinical status of the patient prior to the cardiac arrest

Point To Note

• VF or asystole without CPR within the first 4 to 6 min has a poor outcome, and there are few survivors among patients who had no life support activities for the first 8 min after onset

General Management

• Defibrillate (if indicated)

• AIRWAY

• BREATHING

• CIRCULATION

• ALS Measures

In A WITNESSED Arrest

• A praecordial “thump” delivered to the junction of the middle and lower third of the sternum may occasionally revert VT or VF

• It may convert VT to VF

• Works by delivering a 4J shock

BLS vs ALS

• BLS = EAR + ECC = CPR – (A,B,C)

• ALS = BLS + Advanced Airway Management

IV meds

Defibrillation

Fluids

Defibrillation• When?

– VF/pulseless VT– Torsades– ? Asystole / fine VF (often post adrenalin)

• How much?– 200/200/360 (mono)– 120-150 (biphasic) can max to 200– Biphasic may have less post-resus myocardial dysfunction

(less energy/thermal effects)

• When to sync?

Defibrillation

• Paddle position– Where should they be?

Expired Air Resuscitation (EAR)

• “Mouth to Mouth”

• Bag mask….Aim 6-7 ml/kg TV– Usually 100% O2 (EAR a misnomer here)

– LOS tone less… more TV increases risk of gastric inflation

– Difficult to be accurate

• If you cant intubate, don’t waste time trying

External Cardiac Compression (ECC)

• Current ratio is 15:2 with one OR two operators

• Compression rate 100/min– Improves Coronary Perfusion Pressure– Improves success of defibrillation

EAR + ECC = CPR

• Rate of respiration = 12-15/min– otherwise may cause positive pressure in the

chest and impair the venous return generated

• Must allow chest to recoil fully during ECC– to gain full benefit of negative pressure

• ECC deliver about 1/3 normal SV

• Start without delay– Don’t wait for the defibrillator

IV Access

• Central line best– direct access to heart

• Often peripheral access only one available– Best is antecubital fossa or EJV

• Avoid veins below the diaphragm and distal to the antecubital fossa

• Lots of flushes

Most Commonly Used Drugs

• Adrenaline• Atropine• Amiodarone• Adenosine• Lignocaine• Sotalol

• NaHCO3

• CaCl2

– Hypocalcaemia

– Hyperkalaemia

– Ca++ channel blocker OD

• MgSO4

– Torsades

– Refractory VF

Adrenalin

• Mainstay of drug therapy

• Naturally occurring inotropic agent

• Both and effects

• Positive inotrope

• Increases SVR (and afterload)

• Short acting

• Can be given via ETT if no IV access

Adrenalin

• Increasing doses (cumulatively) may produce poor neurological outcomes post VF arrest– May be as low as 6mg– If given 3-5 minutely, may be a time factor

Atropine

• Anticholingeric

• Increases heart rate

• Useful in bradycardia

• May be of use in asystole (after adrenalin)

• Give enough– at LEAST 300 mcg (usually 500mcg to 1mg)– Otherwise may get paradoxical effects

• Can be given via ETT if not IV access

Amiodarone

• Anti Arrhythmic

• Useful in refractory VF or Pulseless VT

• Give 300mg as bolus– Then an infusion

Adenosine

• Useful in SVT

• May be helpful in obtaining the diagnosis

• Ultra short acting

• Must be followed by large bolus flush

Lignocaine

• Local anaesthetic

• Membrane stabilizing properties

• Dose 1mg/kg– for refractory VF/VT

Vasopressin• Potent endogenous vasoconstrictor

• Unsure of its value

• Levels found to be higher in patients in whom CPR effective (rather than died)

• Improves Coronary Perfusion Pressure– (Diastolic aortic pressure - diastolic RAP)

• Improves Cerebral O2 delivery

• May have better neurological recovery

• May be of use in catecholamine resistance

• Its use is still under investigation

Goals In A Cardiac Arrest

• Restore spontaneous pulse

• Restore BP

• Aim for no neurological deficit

• Know when to STOP